DYNAMICS OF LARGE DENSE-CORED VESICLES IN SYNAPTIC BOUTONS OF THE CATSUPERIOR CERVICAL-GANGLION

We have shown previously that stimulation of the cat cervical sympathe tic trunk for 2 h at 40 Hz depletes the large dense-cored vesicle stor e in synaptic boutons of the superior cervical ganglion and that post- depletion recovery of the store takes several days. In the present stu dy, we examine the properties of the depletion and recovery mechanisms . Invaginations of the plasmalemma suggestive of the exocytosis of den se cores were seen frequently in boutons from stimulated ganglia. The depletion process is calcium dependent: in ganglia perfused with calci um-free Krebs solution no depletion was produced by 40 Hz preganglioni c stimulation. The depletion process is rapid: during continuous stimu lation of the cervical sympathetic trunk with 40 Hz, depletion observe d by the end of 2 h was similar to depletion by the end of the initial 5 min of stimulation. The depletion process is frequency dependent: w hen the cervical sympathetic trunk was stimulated with a constant numb er of stimuli, no depletion occurred at the frequency of 2 or 10 Hz, w hile the frequencies of 20 and 40 Hz produced depletion, which was gre ater at 40 Hz. Recovery of the large dense-cored vesicle store during the initial 24 h after 10 min of 40 Hz stimulation was faster, and of approximately the same magnitude, than during the succeeding five days . Recovery of the store after stimulus-evoked depletion was prevented by application of colchicine to the cervical sympathetic trunk, which suggests dependence of recovery on fast axonal transport. Large dense- cored vesicles accumulated in the colchicine-treated segment of cervic al sympathetic trunk axons. In conclusion, these observations suggest that the stimulus-evoked depletion of large dense-cored vesicle stores in synaptic boutons of the cat superior cervical ganglion is the resu lt of calcium-dependent exocytosis of the large dense-cored vesicle co re and that the post-stimulus recovery is critically dependent on micr otubule-mediated axonal transport.